Archive for February, 2018

One car company recalls 100s of thousands of cars for faulty equipment issues in recent years . It goes on to add , beware , it’s potentially dangerous . . . please fix it and bring your car at the earliest !

Please search for the junk knowledge and then go on to expose, erase and , . . . and throw it to dustbin ! After all , research is searching for truth , again and again !

Let us welcome a new era , where we shall get alerts about wrong knowledge withdrawals and reversal ! Let it challenge the self proclaimed sancto-scientific medical world and a new medical literature cleansing movement (MLCM) begin in every sub specialty.

Conquering left main disease is considered as crowning glory for the Interventional cardiologists. For over three decades , CABG has remained the undisputed modality which is being challenged today. Fortunately, the Incidence of true isolated left main disease is low .(If Medina bifurcation subset is excluded)

With growing expertise , advanced hardware and Imaging ( like a 360 degree OCT fly through view ) one can virtually sit inside the left main and complete a PCI .

Still , coronary care is much . . . much . . . more than a technology in transit !

Most importantly, these complex PCIs require rigorous maintenance protocol with meticulous platelet knockout drugs , patient compliance and the genetic fate of drug efficacy . (Clopidogrel has since entered the final laps of inefficiency while Ticagrelor has some more time I guess !)

What is the current thinking about unprotected left main PCI ? Let us know it from real life experts !

Some of us also suffer from a knowledge gap and tend to think Bifurcation lesions and left main disease are two distinct entities .The fact of the matter is , significant subset of bifurcation lesions are Indeed either left main equivalents or true left mains ( Medina 1,1,1 would constitute > 50 % all bifurc lesions ) If you include Invisible left main lesions in Medina ( 0,1,1 or 0,0,1 ) detected by IVUS/OCT it might reach easily cross 90% (Scientific guess !) Does that mean we have to think CABG even for all complex bifurcation lesions ? and reserve left main disease for isolated discrete mid shaft or ostial left main ?

Final message

My observation (Sincere to my limited conscience !) at least in this part of the world is : Left main Interventions are “perceived as pride” and its more related to “show of expertise”and is little to do with patient outcome.Unfortunately , cardiologists should not be blamed for it in isolation as the studies they follow are conflicted.

Forget SYNTAX/PRECOMBAT trials, the two famous studies EXCEL (Favor PCI) and NOBLE were published in 2016 made our life tough .One suggested PCI is acceptable /on par with CABG, while the other one put CABG superior , ensuring clarity replaced with confusion ! When we have a dispute , logic would suggest we should fall back on the status quo ie “CABG is superior” unless proved convincingly. Many sections of cardiology society failed to appreciate this.

Post PCI thoughts

*It may not be that hard to do a complex PCI . But, it’s never easier to understand current cardiology literature that is supposed to raise our intellect , which has a direct relevance to patient welfare. Note, many crucial , high stake studies tend to play academic deceit games with linguistic and statistical hyperboles like Non Inferior , likely superiority , Never inferior , near equipoise , regression of hazards, virtual follow-up in real vs trial world etc , etc !

I can only hope for a better scientific world !

Reference

Which is the best option for left main disease PCI or CABG ? Journal of Individual wisdom and evidence based conscience : Volume 1 Chapter 1- Coronary Intellect : Pages 0 to ∞ Jan 2018.

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Though PTMC in the presence of LA clot is an option in low risk clots , my strategy would be the last one ,whenever feasible. Intensive, monitored Heparin /Oral anticoagulants ( Heparin 5000 units tds or qid or Low molecular weight heparin Enoxaparin 40-60mg twice a day , Tablet Warfarin /Acitrom with an INR of 3 ) will dissolve LA clot in 30-50% of times.(Our experience).

The percutaneous clot retrieval system is not available as on 2018.Aortic filters are FDA approved during TAVR. (Why not use the same in PTMC ?) LA Catheter based regional lysis through PFO is can be an option if patient agrees to the risk.

How long to wait for clot dissolution with Heparin /OAC?

Most small clots or intermediate sized clots ((Up to 2 CM ?) have been dissolved by 3 months. Even large clots gets dissolved at least in few Instances.Please note, this strategy is applicable only with valves that is fit for PTMC. All others are referred for surgery.

How does heparin lyse a clot ?

Its a miracle to see it happen, though heparin / OAC are never considered as thrombolytic agents .It happens because both heparin and OAC tilts the local endogenous fibrinolytic forces and thrombus melts , dissolves or disappear altogether. (I am waiting for the day , the scientific community to re-label heparin as a thrombolytic agent, Indirectly though !)

Is there a risk of dislodgement of LA clot during heparin /OAC therapy ?

This question shall be addressed to God ! It all happens if bad luck strikes you and your patient.

Be wise . . . and call your surgeon Immediately when you encounter something like this !

Even if the valve is perfectly eligible for PTMC , high risk mobile clots, history of embolic episodes , probing and hyper-googling patients , its better to refer for surgery Immediately. Wait and watch game has a definite risk of stroke and it is especially bound to happen if your patient or their family is anxious !